巨噬细胞炎症状态与过氧化物酶体增殖的相关性研究

The Relationship between Macrophages Inflammation and Peroxisome Proliferation

肥胖引起巨噬细胞浸润机体组织,诱发慢性低度炎症反应,是形成胰岛素抵抗的重要诱因。因此研究影响巨噬细胞炎症状态的因素,有助于深入了解胰岛素抵抗的形成机理。该文通过免疫荧光、Real-time PCR等技术,研究巨噬细胞炎症状态与胞内过氧化物酶体数量之间的关系。结果表明,当巨噬细胞极化为炎症状态的M1型,胞内过氧化物酶体数量变化不显著;当巨噬细胞极化为抗炎状态的M2型,胞内过氧化物酶体数量显著升高。当饱和脂肪酸诱导巨噬细胞极化为炎症状态的类M1型,胞内过氧化物酶体数量变化不显著;当不饱和脂肪酸诱导的抗炎症状态的类M2型,胞内过氧化物酶体数量显著升高。此外,使用过氧化物酶体增殖缺陷型(Pex3–/–)巨噬细胞重复上述实验,也可以极化为M2/类M2型,呈现抗炎状态,但胞内过氧化物酶体数量无显著变化。综上所述,该研究发现巨噬细胞M2/类M2型极化能够诱导胞内过氧化物酶体增殖,但过氧化物酶体增殖不是M2/类M2型极化的必要条件。

Obesity-induced macrophage infiltration into the tissues could lead to chronic low-grade inflammatory or even insulin resistance.Identifying factors that influence the macrophage inflammatory state would thus shed lights on the pathogenesis of insulin resistance.In this study,we investigated the relationship between macrophage inflammatory status and the number of peroxisomes on three sets of systems using techniques including immunofluorescence and Real-time PCR.Results showed that when macrophages polarized to M1(pro-inflammatory),the number of peroxisome did not change significantly,while macrophages polarized to M2(anti-inflammatory),the number of peroxisome increased significantly.These unexpected results were also observed when macrophages polarized in the presence of fatty acids.No significant peroxisome proliferation was observed when macrophages polarized to M1-like by the stimulation of saturated fatty acids,yet peroxisome proliferated significantly when macrophages polarized to M2-like by the stimulation of unsaturated fatty acids.The last set of experiments was carried out on Pex3–/–macrophages,where the peroxisome proliferation was restrained Pex3–/–macrophages could still polarize to anti-inflammatory M2/M2-like status,yet without any noticeable peroxisome proliferation.In conclusion,this study indicated that macrophages M1/M1-like polarization does not induce significant peroxisome proliferation,and M2/M2-like polarization could induce peroxisome proliferation under certain conditions.